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Departments of 1 Anesthesiology and Critical Care Medicine and 2 Pediatrics, The Johns Hopkins University, Baltimore, Maryland 21287; and the 3 Department of Pediatrics, University of Washington, Seattle, Washington 98195
The increase in cerebral blood
flow (CBF) during hypoxia in fetal sheep at 0.6 gestation is less than
the increase at 0.9 gestation when normalized for differences in
baseline CBF and oxygen consumption. Nitric oxide (NO) synthase (NOS)
catalytic activity increases threefold during this period of
development. We tested the hypothesis that administration of the NOS
inhibitor N
-nitro-L-arginine
methyl ester (L-NAME) decreases the CBF response to
systemic hypoxia selectively at 0.9 gestation. We also tested whether
any peripheral vasoconstriction during hypoxia is potentiated by
L-NAME at 0.9 gestation. Administration of
L-NAME increased arterial blood pressure and decreased
microsphere-determined CBF during normoxia in fetal sheep at both 0.6 and 0.9 gestation. With subsequent reduction of arterial oxygen content
by ~50%, the percent increase in forebrain CBF in a control group
(57 ± 11%; ± SE) and L-NAME-treated group (51 ± 6%) was similar at 0.6 gestation. Likewise, at 0.9 gestation, the
increase in CBF was similar in control (90 ± 25%) and
L-NAME (80 ± 28%) groups. At 0.9 gestation,
L-NAME treatment attenuated the increase in coronary blood
flow and increased gastrointestinal vascular resistance during hypoxia.
We conclude that NO exerts a basal vasodilatory influence in brain as
early as 0.6 gestation in fetal sheep but is not an important mechanism
for hypoxic vasodilation in brain at either 0.6 or 0.9 gestation. Thus
the developmental increase in NOS catalytic capacity does not appear to
be responsible for developmental increases in the CBF response to
hypoxia during this period. In contrast, NO modulates the vascular
response to hypoxia in heart and gastrointestinal tract.
cerebral blood flow; coronary blood flow; fetus; gastrointestinal blood flow; sheep
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